It is well known that young organisms do not maintain memories as long as adults, but the mechanisms for this ontogenetic difference are unknown. Our overall research program is to identify the behavioral and molecular mechanisms of these ontogenetic differences. This work is significant because, even though young animals forget more rapidly than adults, early learning and especially traumatic experiences can have consequences that last a lifetime. In this proposal we focus on a molecular cascade that has a significant impact on spine density, as well as trafficking of synaptic markers within these spines. We hypothesize that the fear memory involves the specific activation of both PI3 and MAP kinase through Ca+ influx leading to increased PKM? expression and trafficking AMPA receptors into the synaptic membrane forming protein clusters. Clusters stabilize the AMPA receptor and spine head to maintain the fear memory. Thus, the low activity of PI3 and MAP kinase and the low density of mature spines in juvenile rats reduce both the synthesis of PKM?, its post-translational trafficking (of AMPA receptors), and clustering activities that are paramoun for the rapid consolidation of a fear memory. Our model system utilizes rats of two ages (juveniles and adults) exposed to a potentially life- threatening predator odor in a particular context. Behavioral responses are correlated with neurobiological changes in spines and synaptic markers. We know that juvenile rats show a fear memory 1d after training but not 4d after training. We use this significant time window (1d and 4d post training) to establish the neural mechanisms underlying the differences between ages in retaining the fear memory (Aim 1). In Aim 2, we focus on manipulating the fear memory strength in the juvenile rat. We know that propranolol, a ?-adrenergic receptor antagonist, will block the 1d fear memory in juveniles. Alternatively, we also know that context re- exposure without odor can extend the juvenile fear memory via reconsolidation. We propose to use both propranolol to block fear memory, and context re-exposure trials to extend fear memory in juvenile rats as a behavioral manipulation to assess changes in spine morphology and their underlying neural mechanisms. We propose the following two aims: Aim 1. Identify the role of the PI3-MAP kinase cascade and increasing GluA2 trafficking in mature spines during fear memory formation and retention in juvenile and adult rats. Aim 2. Determine the effect that blocking fear memory and strengthening fear memory has on the activation of the PI3-MAP kinase cascade and GluA2 trafficking in mature spines in juvenile rats. In sum, understanding of the mechanisms through which young animals maintain fear memories over the more pervasive infantile amnesia will be instrumental in developing therapeutic strategies for the prevention of long-lasting intrusive memories in children suffering from anxiety disorders, as well as post- traumatic stress disorder.